The beneficial effect of physical activity (PA) on the brain has been well established. Both acute and regular PA can boost a range of cognitive functions and enhance mood and mental health. Notably, the effect of acute PA on the brain and cognitive functions is generally found to be dose-dependent, in terms of both the amount and intensity of the exercise episode. In contrast, in the case of regular PA, the literature has primarily focused on the amount of exercise, and limited studies have assessed the influence of the exercise intensity. Since PA in higher intensity causes more extensive, more powerful, and longer-lasting neurobiological changes, it may prove more beneficial to cognitive functions and mental health. In the present study, we set out to test this hypothesis by employing a battery of questionnaires and laboratory tests with a sample of young adults. We found that more frequent vigorous- and moderate-intensity PA rather than walking (considered low to moderate intensity) was associated with better cognitive and mental health measures. Meanwhile, compared with no moderate- to vigorous-intensity physical activity (MVPA) at all, as few as 1~2 days per week (lasting at least 10 min each time) of MVPA was associated with a variety of benefits, particularly related to coping with challenging situations. In light of the neurobiological literature, the present study speaks to the value of moderate- to vigorous- rather than low-intensity PA in enhancing cognitive functions and mental health.

Physical activity (PA) significantly influences emotional wellbeing, from enhancing mood to counteracting emotional disorders such as depression and anxiety. This article offers an in-depth analysis of the neurobiological processes and theories underpinning the emotional benefits of PA which arise from exercise-induced physiological changes that simultaneously benefit brain function. We discuss the role of growth factors, neurotransmitters and biochemicals, as well as enhancements in mitochondrial biogenesis and antioxidant activity, and how they foster exercise performance and emotional health. Central to our discussion are theories related to depression: the "neurotrophic," "neurogenesis," "inflammation," "oxidative stress," and "monoamine" hypotheses. We also introduce the emergent "glutamate hypothesis" and discuss exercise-induced lactate release as a potential precursor for glutamate. Additionally, we explore the "endorphin" and "endocannabinoid" hypotheses, underscoring their implications in evoking feelings of euphoria, pain relief and diminished anxiety after exercise. In conclusion, PA exerts a diverse influence on brain health and emotional wellbeing. The dynamic interplay between PA and neurobiological processes signals a promising avenue for future research, with the potential to introduce innovative therapeutic strategies for emotional disorders.

Despite the well-documented beneficial effect of exercise on stress coping and depression treatment, its underlying neurobiological mechanism remains unclear. This is further complicated by a 'side effect' of exercise: it increases basal glucocorticoid (CORT), the stress hormone, which has been shown to be a mediator linking stress to depressive disorders. Here we show that three weeks of voluntary wheel running reduced rats' immobility in the forced swim test (FST), an antidepressant-like effect. Monitoring extracellular fluids in the medial prefrontal cortex PFC (mPFC) using microdialysis we found that, wheel running was associated with higher baseline CORT, but lower FST-responsive CORT. Further, wheel running resulted in a higher dopamine (DA) both at baseline and following FST. Interestingly, the antidepressant-like effect of wheel running was completely abolished by intra-mPFC pre-microinjection of a D2R (haloperidol) but not D1R (SCH23390) antagonist, at a dose that does not affect normal rats' performance in the FST. It suggests that exercise exerts antidepressant-like effect through upregulated DA and in a D2R dependent way in the mPFC. Importantly, the antidepressant-like effect of wheel running was also abolished by intra-mPFC pre-microinjection of a GR antagonist (RU486). Finally, intra-mPFC pre-microinjection of RU486 also downregulated the originally elevated basal and FST-responsive DA in the mPFC of exercise rats. These results suggest a causal pathway linking CORT, GR, DA, and D2R, to the antidepressant-like effect of exercise. In conclusion, exercise achieves antidepressant-like effect through the CORT-GR-DA-D2R pathway and that the increased basal CORT by exercise itself may be beneficial rather than detrimental.